This document discusses destructive lesions of the palate that can arise from various pathological conditions. It begins by describing the anatomy and histology of the palate. It then examines early and late presentations of palatal perforations and the clinical assessment, diagnosis, and classification of different types. Specific conditions that can cause palatal perforations are explored in depth, including cocaine abuse, syphilis, tuberculosis, leprosy, mucormycosis, actinomycosis, and various other infectious, inflammatory, and neoplastic etiologies. The management of many of these conditions is also reviewed. In conclusion, the document emphasizes the importance of a thorough history and laboratory workup to establish an accurate diagnosis for palatal

1. DESTRUCTIVE LESIONS OF
PALATE
Presented by
N.Narmatha
II YEAR PG

2. INTRODUCTION
• The palate is an integral part of the oral cavity constituting
various tissue types that give rise to different types of
pathological conditions.
• Palatal perforation can be defined as a communication between
the nasal cavities and the oral cavity.
• Can pose a difficult diagnostic dilemma for the clinician

3. • It forms both the roof of the mouth and the floor of the nasal
cavity
• Reflecting this, the superior and inferior palatal surfaces have
different mucosae:
• Superior aspect of palate (nasal cavity) – respiratory
epithelium.
• Inferior aspect of palate (oral cavity) – oral mucosa,
populated by secretory salivary glands

4. HISTOLOGY
• Keratinizing stratified squamous epithelium - ortho- or
parakeratinized - explain the decreased incidence of
squamous cell carcinoma in the hard palate as compared to
other areas of the oral cavity

5. EARLY PRESENTATION
• Pain and discomfort
• Ulceration, foul odour and bleeding
Late presentation
• Extension superiorly into the maxillary antrum and nasal cavity
• Nasal obstruction
• Posterior extension into the structures of the oropharynx, into
pterygoid muscles

6. CLINICAL ASSESSMENT
• History and thorough head and neck exam
• Lymph nodes in neck
• Middle ear effusion
• Extension into nasopharynx
• Absent trigeminal blink reflex or palatal hypaesthesia

7. DIAGNOSIS
• CT scan
• MRI
• Biopsy
• FNA

8. CLASSIFICATION
Developmental Cleft palate
Drug related Narcotics (cocaine, heroin etc.,)
Trauma Iatrogenic, Thermal
Infection Tertiary Syphilis, Tuberculosis, Leprosy,
Typhoid, Mucormycosis, Actinomycosis,
Aspergillosis, Paracoccidioidomycosis,
Histoplasmosis, Naso-Oral Blastomycosis,
Leishmaniasis, Diphtheria, Rhinoscleroderma
PATIL SR (2016) PROPOSED CLASSIFICATION FOR THE PALATAL PERFORATION” (DR. SANTOSH PATIL CLASSIFICATION). J INTERDISCIPL MED
DENT SCI 4: 192

9. CONTD……
Neoplasia Lymphoma, Carcinoma, Melanoma, Acute
Lymphoblastic Leukemia
Collagen
vascular disease
Wegener's granulomatosis, Systemic lupus
erythematous
Idiopathic Midline lethal granuloma
Granulomatous
disease
Sarcoidosis, Crohns’s disease
Other Rhinoliths
PATIL SR (2016) PROPOSED CLASSIFICATION FOR THE PALATAL PERFORATION” (DR. SANTOSH PATIL CLASSIFICATION). J INTERDISCIPL MED
DENT SCI 4: 192

10. COCAINE-INDUCED PALATAL PERFORATION
• Coca leaves (erythroxylon coca), the source of cocaine
• Purified chemical, cocaine hydrochloride- isolated from the plant
• Local complications
• Chronic rhinitis
• Sinusitis
• Epistaxis
• Ossification or necrosis of the
nasal septum
• palatal perforation
• Cocaine - potent vasoconstrictor- ischemia - necrosis- ulceration

11. PALATAL PERFORATIONS SECONDARY TO INHALED COCAINE ABUSE. PRESENTATION OF FIVE CASES
Vasoconstrictive and caustic effect of the drug
direct irritation
ischemia of the nasal and palatine mucosa
secondary to maxillary bone destruction
creation of an oronasal perforation

12. Management
• Antibiotics, analgesics
• Prostheses (obturators)
• Surgical reconstructions of the defect
• Nasal septal button
INSERTION OF NASAL SEPTAL BUTTON IN THE TREATMENT OF SEPTAL PERFORATION : A CASE REPORT - SEMANTIC SCHOLAR

13. SYPHILIS
• Syphilis - sexually transmitted infection- bacterium Treponema
pallidum
• Primary stage - single chancre - a firm, painless, non-itchy skin
ulceration but there may be multiple sores
• Secondary syphilis - diffuse rash - palms of the hands and soles of
the feet , sores in the mouth or vagina

14. • In latent syphilis - few or no symptoms
• In tertiary syphilis- gummas (soft, non-cancerous growths)
neurological problems, or heart symptoms
• Gummata - ulcerated nodular granulomatous lesions - causing
localised destruction and perforation of the palate and
lobulated enlargement and surface irregularities of the tongue

15. CONTD…..

16. MANAGEMENT
Recommended Regimen for Adults
• Benzathine penicillin G 2.4 million units IM in a single dose
• Infants and Children - 50,000 units/kg IM - 2.4 MU
Penicillin Allergy
• Doxycycline 100 mg orally bid - 14 days
• Tetracycline (500 mg four times daily for 14 days)
Tertiary Syphilis
• Benzathine penicillin G 7.2 million units total, 3 doses of
2.4 million units IM each at 1-week intervals
• June 4, 2015Content source: Division of STD Prevention, National Center for HIV/AIDS, Viral Hepatitis, STD, and TB Prevention, Centers for Disease Control and
Prevention

17. TUBERCULOSIS
• Tuberculosis (TB) - caused by Mycobacterium tuberculosis
• Pulmonary TB - most common form
• Both primary and secondary types of TB - cause lesion in the
oral cavity.
• In secondary TB, lesions of the oral cavity may accompany
lesions in the pharynx, lungs, lymph nodes and skin
PRIMARY TUBERCULOSIS OF PALATE

18. • Oral TB is rarely seen
• Few factors that attribute to relative resistance of oral cavity TB
are
• protection by the oral saliva,
• presence of saprophytes,
• resistance of the striated muscles to bacterial invasion
• thickness of the protective epithelial covering

19. • The most common site for oral TB - tongue
• Others - soft palate, hard palate, lip, cheek, tonsils,
gingiva, floor of the mouth, uvula, and alveolar mucosa.
• Manifestation of oral TB is an ulcerative lesion of the
mucosa.

20. opalescent vesicle or a nodule
caseation necrosis
ulcer
• A typical TB lesion - ragged undermined edges, minimal
induration and often with a yellowish apple jelly like
granular base - ulcerate leaving radiating scars.
PRIMARY TUBERCULOSIS OF PALATE

21. DIAGNOSIS
• Can mimic a malignant neoplasm
• Primary lesions of TB manifest in the oral cavity
as non-healing chronic ulcers.
• Chest radiograph and tissue biopsy for histological
studies

22. Management:
• Isoniazid – 300 mg twice weekly
• Rifampicin – 600 mg
• Rifabutin – 300 mg
• Pyrazinamide - 2g
• Ethambutol – 1.6 g

23. LEPROSY
• Leprosy is a chronic infectious disease - Mycobacterium
leprae
• Two forms - lepromatous and tuberculoid forms
• Mainly it affects skin, peripheral nerves and nasal mucosa
• It can also affect the oral cavity

24. • Oral lesions are more common in lepromatous type of
leprosy.
• In the oral cavity, it can involve the palate, buccal
mucosa, tongue
• M. leprae prefer to colonize the cooler parts of the body
• The commonest site of oral cavity - hard palate >soft
palate, labial and buccal maxillary gingiva, tongue, lips,
labial mandibular gingiva > buccal mucosa.

25. palate
ulceration
perforation
oro-nasal fistula
• Erythema nodosum leprosum is an important but rare cause of the
destruction of the hard and soft palate
• Palatal nodulo ulcerative lesions of leprosy may mimic squamous
cell carcinoma

29. MUCORMYCOSIS
COTRAN, KUMAR, ROBBINS ROBBINS' PATHOLOGIC BASIS OF DISEASE, (4'° SUB ED.) WB SAUNDERS AND CO, PHILADELPHIA, 356,1989
• Opportunistic fungal infection - caused by normally saprobic
organism of the class Zygomycetes
• Invasion of surrounding tissue - necrotizing ulceration of palate
with a blackish slough and exposure of bone

30. • The 5 major clinical forms are as follows:
1. Rhinocerebral
2. Pulmonary
3. Abdominal pelvic and gastrointestinal
4. cutaneous
5. Disseminated forms
• Rhinocerebral mucormycosis – typically commences in
the nasal cavity or paranasal sinuses – invade the palate
(black necrotic ulceration)

31. EARLY DIAGNOSIS OF MUCORMYCOSIS

32. Lab investigation:
• Direct morphologic identification of mycotic elements and
recovery of Mucorales organisms in culture from specimens
• Histologic examination - periodic acid-Schiff and Gomori
methanamine silver stains

34. ACTINOMYCOSIS
• Slowly progressing infection caused by anaerobic bacteria
Actinomyces
• Three distinct clinical forms
• Cervicofacial
• abdominopelvic
• Thoracopulmonary
• Destroy local tissue in a highly vascularised and therefore
aerobic region and replaces it with granulation tissue.

35. Treatment :
IV penicillin -2-4 weeks – 6-12
months

36. WEGENER’S GRANULOMATOSIS
• Rare chronic granulomatous disease
• Immunological
• C/F : Necrotizing granulomatous lesions of the respiratory
tract ,generalized focal necrotizing vasculitis and necrotizing
glomerulonephritis.

39. • Oral manifestation : solitary or multiple irregular ulcers,
surrounded by an inflammatory zone
• Tongue, palate ,buccal mucosa and gingiva.
• Lab investigation: c-ANCA –anti neutrophil cytoplasm test

41. 1.5 – 2 mg/kg
7– 15mg/kg
2 mg/kg ,1.5 mg,1
mg/kg

42. SARCOIDOSIS
• Systemic granulomatous disease
• Non caesating granuloma – characteristic lesion.
• Oral manifestation: multiple, nodular, painless ulceration of the
gingiva, buccal mucosa, tongue, lips and palate

45. MIDLINE LETHAL GRANULOMA
• Lethal midline granuloma (LMG) is an historical term for
a condition in which necrotic and highly destructive lesions
develop progressively in the middle of the face, principally
the nose and palate

46. • Manifestation of three or four different diseases:
• the well-characterized disease of granulomatosis with
polyangiitis
• the ill-defined disorders of polymorphic reticulosis
• mid-line malignant reticulosis,
• and an incompletely defined form of non-Hodkgins
disease malignant lymphoma

47. MANAGEMENT

48. NOMA
• Noma is a rapidly progressive, polymicrobial, often
gangrenous infection of the mouth or genitals.

49. • The mucous membranes of the mouth develop ulcers - rapid,
painless tissue degeneration - degrade tissues of the bones in the
face
• Bacterial cause:
Fusobacterium necrophorum and Prevotella intermedia (such
as Borrelia vincentii, Porphyromonas gingivalis, Tannerella
forsythia, Treponema denticola, Staphylococcus aureus, and
certain species of nonhemolytic Streptococcs).

50. NECROTISING SIALOMETAPLASIA
• Uncommon locally destructive inflammatory condition of the
salivary glands
• Cause: unknown
• Result of ischemia of the salivary tissue
that leads to local infarction.

52. • Benign, ulcerative lesion, usually located towards the back
of the hard palate.
• It is thought to be caused by ischemic necrosis (death of
tissue due to lack of blood supply) of minor salivary
glands in response to trauma.

53. CLINICAL FEATURES
• Most frequently develops in palatal salivary glands
• Hard palate> soft palate
• 2/3 of palatal cases are unilateral ,with the rest being
bilateral or midline in location
• Appears initially as non- ulcerated swelling often
associated with pain or parasthesia with crater like ulcer
<1cm >5cm in diameter appearing within 2-3 weeks.

54. • Investigation: biopsy
• Management : Irrigation, self limiting disorder

55. PHOSSY JAW
• Phossy jaw, formally known as phosphorus necrosis of the
jaw
• an occupational disease affecting those who worked with white
phosphorus
• white phosphorus vapour- destroys the bones of the jaw

56. Treatment:
• Topical antimicrobials
• Conservative debridement of sequestra
• Surgical removal of the afflicted jaw bones
Diagnosis:
• In radiographs, the sequestra present as a typical worm-eaten
appearance. Sequestra appear osteoporotic and decalcified.
Separation of the dead bone from the surrounding bone appears
clearly demarcated in the radiographs

57. TUMORS OF THE PALATE
• Palate - most common site for minor gland neoplasms.
• Cancer of the soft palate - 2% of head and neck mucosal
malignancies.
• Hard palate cancers are squamous cell carcinomas (SCCs)

58. • Non squamous cell cancers - minor salivary gland cancers,
sarcomas, and melanomas.
• Benign tumors - pleomorphic adenomas
• Malignant tumors - mucoepidermoid carcinoma, adenoid cystic
carcinoma, and polymorphous low-grade adenocarcinoma.

59. BENIGN PLEOMORPHIC ADENOMA
• Most common benign mixed tumor composed of epithelial
and myoepithelial cells arranged with various
morphological patterns, demarcated from surrounding
tissues by fibrous capsule.

60. MALIGNANT SQUAMOUS EPITHELIAL
NEOPLASMS
MUCOEPIDERMOID CARCINOMA (MEC)
• Arise from pluripotent reserve cells of excretory ducts that
are capable of differentiating into squamous, columnar, and
mucous cells

61. ADENOID CYSTIC CARCINOMA
• Accounts for <1% of all head and neck malignancies
• 4-10% of all salivary gland tumors
• commonest malignant tumor of the minor salivary glands
• Intraorally 50% - occur on the palate

62. POLYMORPHOUS LOW-GRADE ADENOCARCINOMA
• Malignant epithelial tumor
• Characterized by cytological uniformity, morphological
diversity, an infiltrative growth pattern and low metastatic
potential
• Most common location - palate
• More frequent in women

63. CONCLUSION:
It is well understood that the palatal perforation can pose a
difficult diagnostic dilemma for the clinician. The perforation
may present with the common characteristics and may be
indistinguishable clinically. Emphasis is placed on the
importance of obtaining a thorough and comprehensive
history and collecting relevant laboratory information.

64. REFERENCES
1.Textbook of oral medicine ,burkett -11 th edition
2.Oral pathology – shafer’s
3.Cotran, kumar, robbins pathologic basis of disease, (4'° sub
ed.) WB saunders and co, philadelphia, 356,1989
4.June 4, 2015content source: division of STD
prevention, national center for HIV/AIDS, viral hepatitis, STD,
and TB prevention, centers for disease control and prevention

65. Thank you